Assessment of Cardiac, Vascular, and Pulmonary Pathobiology In Vivo During Acute COVID-19

  • Shirjel R. Alam
  • , Sudhir Vinayak
  • , Adeel Shah
  • , Gemina Doolub
  • , Redemptar Kimeu
  • , Kevin P. Horn
  • , Stephen R. Bowen
  • , Mohamed Jeilan
  • , Kuan Ken Lee
  • , Sylvia Gachoka
  • , Felix Riunga
  • , Rodney D. Adam
  • , Hubert Vesselle
  • , Nikhil Joshi
  • , Mariah Obino
  • , Khalid Makhdomi
  • , Kevin Ombati
  • , Edward Nganga
  • , Samuel Gitau
  • , Michael H. Chung
  • Anoop S.V. Shah

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

BACKGROUND: Acute COVID-19– related myocardial, pulmonary, and vascular pathology and how these relate to each other remain unclear. To our knowledge, no studies have used complementary imaging techniques, including molecular imag-ing, to elucidate this. We used multimodality imaging and biochemical sampling in vivo to identify the pathobiology of acute COVID-19. Specifically, we investigated the presence of myocardial inflammation and its association with coronary artery disease, systemic vasculitis, and pneumonitis. METHODS AND RESULTS: Consecutive patients presenting with acute COVID-19 were prospectively recruited during hospital admission in this cross-sectional study. Imaging involved computed tomography coronary angiography (identified coronary disease), cardiac 2-deoxy-2-[fluorine-18]fluoro-D-glucose positron emission tomography/computed tomography (identified vascular, cardiac, and pulmonary inflammatory cell infiltration), and cardiac magnetic resonance (identified myocardial dis-ease) alongside biomarker sampling. Of 33 patients (median age 51 years, 94% men), 24 (73%) had respiratory symptoms, with the remainder having nonspecific viral symptoms. A total of 9 patients (35%, n=9/25) had cardiac magnetic resonance– defined myocarditis. Of these patients, 53% (n=5/8) had myocardial inflammatory cell infiltration. A total of 2 patients (5%) had elevated troponin levels. Cardiac troponin concentrations were not significantly higher in patients with and without myocarditis (8.4 ng/L [interquartile range, IQR: 4.0– 55.3] versus 3.5 ng/L [IQR: 2.5– 5.5]; P=0.07) or myocardial cell infiltration (4.4 ng/L [IQR: 3.4– 8.3] versus 3.5 ng/L [IQR: 2.8–7.2]; P=0.89). No patients had obstructive coronary artery disease or vasculitis. Pulmonary inflammation and consolidation (percentage of total lung volume) was 17% (IQR: 5%– 31%) and 11% (IQR: 7%–18%), respec-tively. Neither were associated with the presence of myocarditis. CONCLUSIONS: Myocarditis was present in a third patients with acute COVID-19, and the majority had inflammatory cell infil-tration. Pneumonitis was ubiquitous, but this inflammation was not associated with myocarditis. The mechanism of cardiac pathology is nonischemic and not attributable to a vasculitic process. REGISTRATION: URL: https://www.isrctn.com; Unique identifier: ISRCTN12154994.

Original languageEnglish (US)
Article numbere026399
JournalJournal of the American Heart Association
Volume11
Issue number18
DOIs
Publication statusPublished - 20 Sept 2022
Externally publishedYes

Keywords

  • CMR
  • COVID-19
  • FDG-PET
  • myocarditis
  • pneumonitis

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